Histopathological characterisation of effects of the mouse Pax6 missense mutation on eye development

Mutations in PAX6/Pax6 lead to a variety of ocular anomalies in humans and mice. The aim of the study was to characterise the ocular abnormalities caused by the missense Pax6^Leca4 mutation and compare them to published observations on Pax6 alleles that are functionally equivalent to Pax6⁻ null alleles (such as Pax6^Sey and Pax6^Sey-Neu) and human inherited eye diseases. Ocular features of homozygous Pax6^Leca4/Leca4 and heterozygous Pax6^Leca4/+ embryos at E12.5-E18.5, heterozygous Pax6^Leca4/+ young mice at P18 and heterozygous Pax6^Leca4/+ adults at 12 weeks were analysed histologically with their wild-type Pax6^+/+ littermates. Homozygous Pax6^Leca4/Leca4 fetuses died perinatally with no eyes although an optic cup rudiment with pigmented cells developed. Pax6^Leca4/+ mice were microphthalmic and a range of other severe ocular phenotypes affected both the anterior and the posterior segments. In contrast to Pax6^+/−, the Pax6^Leca4/+ eyes had no goblet cells in the corneal epithelium, the iris was not hypoplastic and there was no lens-corneal epithelial plug. However, microphthalmia was more severe, corneal vascularisation occurred earlier (during fetal stages), pigmented cells were present in the vitreous and corneal stroma and the ciliary body was malformed or abnormal. These results show that, although Pax6^Leca4/+ lacked some eye abnormalities commonly seen in Pax6^Sey/+ and Pax6^Sey-Neu/+ eyes, in most respects their eyes were more severely affected. These differences probably reflect both differences between the Pax6^Leca4 and the Pax6^Sey-Neu mutations and differences in modifier gene expression in different genetic backgrounds. The presence of pigmented cells in the cornea is a novel observation. Some Pax6^Leca4/+ ocular abnormalities were similar to those present in human Peters' anomaly and persistent hyperplastic primary vitreous (PHPV) so Pax6^Leca4/+ mice provide a useful model for some inherited eye diseases.     

益气复智颗粒对多发脑梗死性痴呆模型大鼠脑组织细胞凋亡的影响

目的 观察益气复智颗粒对多发脑梗死性痴呆模型大鼠脑皮质形态学、细胞凋亡的影响。方法 采用颈内动脉注射血栓的方法，复制多发梗死性痴呆大鼠模型，观察益气复智颗粒12．42g/kg分别于手术前、手术前后、手术后灌胃对实验动物脑皮质形态学、细胞凋亡的影响。结果 益气复智颗粒能使脑缺血后脑内神经细胞凋亡数目下降。结论 益气复智颗粒具有较好的保护脑神经元，阻断脑缺血致神经细胞死亡病理过程的作用。     

关于中成药口腔崩解片开发应用的思考

通过对口腔崩解片的特点及主要制备工艺的分析,结合当前中成药工业的现状及具体实际,认为口腔崩解片可以应用于中成药制剂的开发。     

Contemporary Models of Youth Development and Problem Prevention: Toward an Integration of Terms,Concepts, and Models

Over the past several years, increased interest in preventing youth problems and promoting healthy youth development has led youth and family practitioners, policy makers, and researchers to develop a wide range of approaches based on various theoretical frameworks. Although the growth in guiding frameworks has led to more complex models and a greater diversity in the options available to scholars and practitioners, the lack of an integrative conceptual scheme and consistent terminology has led to some confusion in the field. Here, we provide an overview of three approaches to youth development and problem prevention, critically examine their strengths and weaknesses, and offer some elaborations to help clarify, extend, and integrate the models. We conclude by discussing some general implications for researchers, practitioners, and policy makers.     

梗阻性脑积水侧脑室及室周脑组织生物力学响应的有限元分析

目的运用有限元方法对梗阻性脑积水进行计算机模拟,研究分析侧脑室及室周脑组织的生物力学响应及其所产生的病理生理影响。方法依据正常国人颅脑MRI轴位T2加权图像获取解剖信息,在有限元软件ANSYS中生成包含侧脑室前、后角和体部的半侧脑层面的二维有限元模型。模拟脑组织为固、液两相物质组成的线性多孔弹性材料,设定生物力学特性参数及边界条件和初始条件,施加载荷,运用有限元软件ABAQUS进行计算求解,以云图形式输出结果。结果有限元模型动态模拟了梗阻性脑积水侧脑室各部的扩张过程,直观显示出各个时间步室周脑组织内的应力类型及分布、各部的应变和位移。结论膨胀性应力集中引起角部脑水肿;梗阻性脑积水早期侧脑室角部形态变化最明显;体部附近脑组织结构容易受压移位。这些生物力学响应是室内压增高的结果,也与侧脑室的解剖形态密切相关。     

优化结构提高效率实现医院可持续发展

随着我国医疗保险的大范围实施，医院只有优化结构、提高效率，才能实现可持续发展。以财务管理为出发点，分析了目前大型医院所面临的现行国家医疗政策、外部环境以及内部约束等条件，提出强化医疗业务管理．建立科学合理的医疗业绩考核指标体系：平均住院天数、出院人数、手术量、门诊预约率，促进医疗业绩的提高：强化财务管理，建立现代医院财务考核指标体系：结余率、人均结余、病人人均费用，对各个科室的经济效益进行考核，促进医院经济效益的提高。     

Exo-focal postischemic neuronal damage in the rat brain: alteration of [H]forskolin binding using in vitro autoradiography

We studied the alteration of intracellular signal transduction using quantitative autoradiography of the second messenger system in order to clarify the mechanisms of delayed neuronal damage in the remote areas of rat brain after transient focal ischemia. Chronological changes of [³H]forskolin binding sites were measured to demonstrate the striatal-nigral pathway after 90 min of right middle cerebral artery (MCA) occlusion and after such occlusion followed by 3 h, 6 h, 1 day, 3 days, 1 week, 2 weeks and 4 weeks of recirculation. [³H]Forskolin binding sites were found to be markedly decreased in the lateral segment of the caudate putamen supplied by the occluded MCA after 90 min of ischemia with no recirculation. On the contrary, there was no alteration on day 1, but 3 days after ischemic insult, marked reduction of [³H]forskolin binding sites was observed in the ipsilateral substantia nigra which lay outside the ischemic areas. This postischemic delayed phenomenon observed in the substantia nigra developed concurrently with ⁴⁵Ca accumulation, which was detected there in our previous study. The delayed reduction of [³H]forskolin binding sites in the substantia nigra observed in the present study indicates that striatonigral terminal degeneration at presynaptic sites is caused by precedent ischemic damage of the ipsilateral caudate putamen and that exo-focal postischemic neuronal death is caused by a transsynaptic process associated with the ischemic foci.     

Developmental expression of aldehyde dehydrogenase in rat: a comparison of liver and lung development.

Metabolism is one of the major determinants for age-related changes in susceptibility to chemicals. Aldehydes are highly reactive molecules present in the environment that also can be produced during biotransformation of xenobiotics and endogenous metabolism. Although the lung is a major target for aldehyde toxicity, early development of aldehyde dehydrogenases (ALDHs) in lung has been poorly studied. The expression of ALDH in liver and lung across ages (postnatal day 1, 8, 22, and 60) was investigated in Wistar-Han rats. In adult, the majority of hepatic ALDH activity was found in mitochondria, while cytosolic ALDH activity was the highest contributor in lung. Total aldehyde oxidation capability in liver increases with age, but stays constant in lung. These overall developmental profiles of ALDH expression in a tissue appear to be determined by the different composition of ALDH isoforms within the tissue and their independent temporal and tissue-specific development. ALDH2 showed the most notable tissue-specific development. Hepatic ALDH2 was increased with age, while the pulmonary form did not. ALDH1 was at its maximum value at postnatal day 1 (PND1) and decreased thereafter both in liver and lung. ALDH3 increased with age in liver and lung, although ALDH3A1 was only detectible in lung. Collectively, the present study indicates that, in the case of aldehyde exposure, the in vivo responses would be tissue and age dependent.